Yujun Li1,2, Junrong Liang3, Hui Dang1, Rui Zhang1, Pu Chen1, Yuan Shao4. 1. Department of Endocrinology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, PR China. 2. Department of Endocrinology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, PR China. 3. Department of Gastroenterology, Tangdu Hospital, Fourth Military Medical University, Xi'an, 710038, PR China. 4. Department of Otolaryngology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, PR China. shaxiaoying1976@163.com.
Abstract
PURPOSE: The Nuclear Receptor Coactivator (NCOA3, also known as SRC-3, AIB1, p/CIP, RAC3, ACTR, and TRAM1), acts as an oncogene in multiple tumors, but its biological function in thyroid cancer remains unclear. This study was designed to explore the role of NCOA3 in thyroid cancer. METHODS: The study assessed NCOA3 expression in thyroid cancer and their matched non-cancerous thyroid tissues at mRNA and protein levels. Then we evaluated the effect of NCOA3 on malignant activities of thyroid cancer cells. To better understand the oncogenic role of NCOA3 in thyroid tumorigenesis, we tested the effect of NCOA3 on major proteins related to thyroid cancer. RESULTS: Our data demonstrated that protein expression of NCOA3 was significantly upregulated in thyroid cancer tissues. NCOA3 knockdown inhibited cell proliferation and invasion, and induced cell cycle arrest and apoptosis in thyroid cancer. Conversely, ectopic expression of NCOA3 promoted cell proliferation and invasiveness in thyroid cancer. Mechanistically, NCOA3 could improve the survival and invasiveness of thyroid cancer cells through the modulation of the ErbB, AKT, ERK, and β-catenin pathways. CONCLUSION: Collectively, these findings suggest that NCOA3 is critical in the initiation and development of thyroid cancer, and might be a possible marker for prognosis and therapy.
PURPOSE: The Nuclear Receptor Coactivator (NCOA3, also known as SRC-3, AIB1, p/CIP, RAC3, ACTR, and TRAM1), acts as an oncogene in multiple tumors, but its biological function in thyroid cancer remains unclear. This study was designed to explore the role of NCOA3 in thyroid cancer. METHODS: The study assessed NCOA3 expression in thyroid cancer and their matched non-cancerous thyroid tissues at mRNA and protein levels. Then we evaluated the effect of NCOA3 on malignant activities of thyroid cancer cells. To better understand the oncogenic role of NCOA3 in thyroid tumorigenesis, we tested the effect of NCOA3 on major proteins related to thyroid cancer. RESULTS: Our data demonstrated that protein expression of NCOA3 was significantly upregulated in thyroid cancer tissues. NCOA3 knockdown inhibited cell proliferation and invasion, and induced cell cycle arrest and apoptosis in thyroid cancer. Conversely, ectopic expression of NCOA3 promoted cell proliferation and invasiveness in thyroid cancer. Mechanistically, NCOA3 could improve the survival and invasiveness of thyroid cancer cells through the modulation of the ErbB, AKT, ERK, and β-catenin pathways. CONCLUSION: Collectively, these findings suggest that NCOA3 is critical in the initiation and development of thyroid cancer, and might be a possible marker for prognosis and therapy.
Authors: Nancy L Cho; Chi-Iou Lin; Edward E Whang; Adelaide M Carothers; Francis D Moore; Daniel T Ruan Journal: Thyroid Date: 2010-06 Impact factor: 6.568
Authors: Iñigo Landa; Tihana Ibrahimpasic; Laura Boucai; Rileen Sinha; Jeffrey A Knauf; Ronak H Shah; Snjezana Dogan; Julio C Ricarte-Filho; Gnana P Krishnamoorthy; Bin Xu; Nikolaus Schultz; Michael F Berger; Chris Sander; Barry S Taylor; Ronald Ghossein; Ian Ganly; James A Fagin Journal: J Clin Invest Date: 2016-02-15 Impact factor: 14.808